This could mean that people with the disorder have a harder time discerning truly worrisome situations from mild annoyances.

This study and others also found too much connection with the prefrontal cortex and too much activity there:

At the same time, the amygdala was more connected to a cortical executive-control network previously found to exert cognitive control over emotion.

Something in this circuit between the two areas is off-balance.

Another study found:

The results show that worry in normal subjects and in subjects with GAD is based on activation of the medial prefrontal and anterior cingulate regions, known to be involved in mentalization and introspective thinking. A dysregulation of the activity of this region and its circuitry may underpin the inability of GAD patients to stop worrying

This misrouting may be due to weak connection at one key choke point in this whole fear-rational circuit:

In this case, two types of scans showed the amygdala, which alerts us to threat in our surroundings and initiates the “fight-or-flight” response, seems to have weaker “white matter” connections to the prefrontal and anterior cingulate cortex (ACC), the center of emotional regulation.

the imaging showed the brains of people with GAD had reduced connections between the prefrontal and anterior cingulate cortex and the amygdala via the uncinate fasciculus, a primary “white matter” tract that connects these brain regions.

More importantly…

This reduced connectivity was not found in other white matter tracts elsewhere in their brains.

We discussed the anterior cingulate cortex in our CBD for anxiety article.

The uncinate fasciculus is a new actor though.

The plot thickens.

Research is showing this communication tract between our Amygdala and the prefrontal cortex is critical to anxiety:

The UF-amygdala complex may be pivotal for the control of trait anxiety.

increased frequency of anxiety disorders after TBI may reflect an overlap between brain regions vulnerable to traumatic brain injury, and the neural circuitry of these disorders.

We've talked about some of the circuits at work (amygdala/prefrontal cortex, the uncinate fasciculus, etc).

What about infection and inflammation?

This is where there's really exciting new research.

The tell-tale signs of both (immune response) is all over general anxiety disorder:

analyses revealed significant differences in serum levels of IL-10, TNF-α, and IFN-γ between GAD and control groups after adjusting for age, gender, body mass index, smoking and alcohol consumption: these group differences were independent of the presence or degree of depression.

GAD is general anxiety disorder of course. Those strange chemicals are all inflammatory immune responders.

Did you notice that last little piece…"independent of the presence or degree of depression".

That's really important.

They found these various immune agents elevated for anxiety by itself!

There are dozens are studies like this all pointing in the same direction.

Immune response (which governs how our body deals with both infection and inflammation) is higher in people with general anxiety disorder!

Put a checkmark next to that for when we get to CBD. Very exciting.

One last stop...the gut!

Gut Dysbiosis

This is the new Wild West of health...the trillions of bacteria in our gut.

How does this affect general anxiety disorder?

When they compared healthy people's guts versus those with general anxiety disorder, there were marked differences:

Compared with the HCs, we found markedly decreased microbial richness and diversity, distinct metagenomic composition with reduced short-chain fatty acid (SCFA)-producing bacteria (associated with a healthy status) and overgrowth of bacteria, such as Escherichia-Shigella, Fusobacterium and Ruminococcus gnavus

It was the only area showing reduced activity in the brain scans of people with GAD.

People who use cannabis showed reductions in volume for that very important communication link:

Compared to non-users, CU had worse memory performance, decreased fiber bundle length in the UF, and decreased cortical thickness of brain regions along the UF such as the entorhinal cortex and fusiform gyrus.

It shows that the underlying endocannabinoid system is governed with "balancing" brain signaling for CBD to have this effect.

Remember that the net result of brain injury, inflammation or genetic variations with general anxiety disorder is irregular signalling (not enough GABA, not enough serotonin in specific areas, etc).

The ability of CBD to boost this balancing mechanism is fascinating.

What about actual brain structure? That's a long term consideration with GAD.

Remember how we noted that THC has been shown to adversely affect brain areas?

Most of the research on CBD on brain structure results from its protective role against these changes from THC.

THC's effects are here:

Across the 31 studies selected for inclusion in this review, neuroanatomic alterations emerged across regions that are high in cannabinoid receptors (i.e., hippocampus, prefrontal cortex, amygdala, cerebellum).

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